Calculation of QTc duration and variability in the presence of sinus arrhythmia

doi:10.1016/S0002-9149(99)80697-3

The American Journal of Cardiology

Volume 75, Issue 14, 1 May 1995, Pages 950-952

https://doi.org/10.1016/S0002-9149(99)80697-3 Get rights and content

In summary, this study proposes guidelines for calculation of the QTc in the presence of SA to help identify patients with true LQTS: (1) The QT interval immediately following the shortest RR interval should be used (with Bazett's formula) to calculate the QTc in patients with SA. (2) It is rare to have LQTS with a QTc <0.46 with SA using the shortest RR interval. (3) Varying absolute QT intervals (>0.04 second) with changing RR intervals also are suggestive of LQTS.

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Cited by (24)

Interpretation of the Electrocardiogram in Athletes
2016, Canadian Journal of Cardiology
Citation Excerpt :
Bazett's formula (QTc = QT/√R-R interval) corrects the QT duration for heart rate, however, it is less accurate at extremes of heart rates: with undercorrection for tachycardia > 120 bpm and overcorrection for bradycardia ≤ 40 bpm. In the presence of sinus arrhythmia, it has been found that using the QTc between the shortest R-R interval has a sensitivity of 100% in a nonathletic population (all 63 long QT patients had a QTc > 450 ms, although 1 patient had a QTc < 460 ms) and a false positive rate of 4% (3 of the 80 control subjects had a QTc > 460 ms).48 However, our practice is to use the averages of the QT and R-R intervals, which, although it has a lower sensitivity of 84% (53 of the 63 long QT patients had a QTc > 460 ms), it has a 0% false positive rate (0 of the 80 control subjects had a QTc > 460 ms) in conjunction with assessment of the morphology of the T wave, to prevent an erroneous diagnosis, which might jeopardize the athlete's career.
Regular intensive participation in sport results in electrical and structural alterations within the heart that can manifest on the surface electrocardiogram (ECG). In addition to the actual sporting discipline and the volume and intensity of exercise being performed, other factors play a role in the development of certain ECG patterns including sex, age, and ethnicity. In some instances, large male endurance athletes and those of African or Afro-Caribbean origin (black athletes), might exhibit ECG patterns that overlap with those seen in patients with cardiomyopathy and channelopathies, which are recognized causes of exercise-related sudden cardiac death. The ability to distinguish accurately between benign physiological electrical alterations and pathological ECG changes is crucial to prevent the unnecessary termination of an athlete's career and to minimize the risk of sudden death. Several recommendations currently exist to aid the physician in the interpretation of the athlete's ECG. In this review we discuss which ECG patterns can safely be considered benign as opposed to those that should prompt the physician to consider cardiac pathology.
Une participation intensive et régulière à des activités sportives peut entraîner l’apparition de modifications électriques et structurelles du cœur pouvant être décelées par un électrocardiogramme (ECG) de surface. En plus du type de discipline sportive pratiquée et de la quantité et de l’intensité d’exercice effectué, divers facteurs jouent un rôle dans l’apparition de certains tracés d’ECG, notamment le sexe, l’âge et l’origine ethnique. Dans certains cas, les athlètes de sexe masculin et de grande taille qui pratiquent un sport d’endurance et les athlètes d’origine africaine ou afro-caribéenne (de race noire) peuvent présenter des tracés d’ECG semblables à ceux des patients atteints d’une cardiomyopathie ou d’une canalopathie, lesquelles, on le sait, peuvent entraîner une mort subite d’origine cardiaque liée à l’exercice. La capacité de distinguer clairement une modification électrique physiologique bénigne d’une modification pathologique à l’ECG est cruciale pour éviter de mettre inutilement fin à la carrière d’un athlète et de minimiser le risque de mort subite. Il existe actuellement plusieurs recommandations pour aider le médecin à interpréter les tracés d’ECG d’un athlète. Nous vous présentons dans cet ouvrage une revue des tracés d’ECG qui peuvent d’emblée être considérés comme bénins ainsi que de ceux qui doivent amener le médecin à envisager la présence d’une pathologie cardiaque.
The prevalence and diagnostic/prognostic utility of sinus arrhythmia in the evaluation of congenital long QT syndrome
2010, Heart Rhythm
Citation Excerpt :
Despite these exclusions, LQTS patients (130 of 227, 62%) continued to show SA less frequently than normal subjects (175 of 242, 76%, P = .001). Additionally, to ensure that a different definition of SA would not affect outcome, we used a different calculation method as described by Martin et al,20 in which SA was designated when the maximum RR interval minus the minimum RR interval exceeded 80 ms in a 10-second rhythm strip. Here, 170 of 281 LQTS patients (61%) satisfied this definition of SA compared with 223 of 290 (77%) of normal subjects (P < .0001).
Congenital long QT syndrome (LQTS) affects 1 in 2,500 people and can cause syncope and sudden death. Sinus arrhythmia (SA) is nonpathologic baseline respiratory variation of the RR interval.
This study sought to determine the frequency of SA and its clinical significance among patients with LQTS.
We performed an institutional review board–approved retrospective review of all patients (N = 571) evaluated in our LQTS clinic from 7/2000 to 3/2008 diagnosed with LQTS (N = 281) or dismissed as otherwise normal (N = 290). Blinded to diagnosis, the first available electrocardiogram for each patient was examined to quantitate RR interval variability.
Overall, 151 of 281 patients (54%) with LQTS (159 female patients, average age 21.8 ± 16.5 years, average QTc 466 ± 43 ms) had SA with an average RR variability of 13% ± 8% compared with 201 of 290 (69%) patients dismissed as normal (178 female patients, average age 21.7 ± 16 years, average QTc 424 ± 30 ms) who demonstrated SA with RR variability of 16% ± 10% (P < .0001). These differences remained significant when patients on concurrent beta-blocker therapy were excluded (P < .001). SA was least common in LQT3 (23%) compared with LQT1 (61%, P < .005) and LQT2 (51%, P = .055). Patients presenting with torsades de pointes or aborted cardiac arrest had lower RR variability (10% ± 7%, P < .03).
SA frequency and magnitude of RR variability was lower among patients with LQTS compared with those patients dismissed as otherwise normal. This attenuation in RR interval variability remained when patients on beta-blocker therapy were excluded. Although the presence/absence of sinus arrhythmia is of little diagnostic value due to cohort overlap, LQTS patients with negligible RR interval variation may be at higher risk.
Application of probabilistic analysis for precisely correcting the QT interval for heart rate in telemetered common marmosets
2010, Journal of Pharmacological and Toxicological Methods
Introduction: QT intervals are strongly influenced by preceeding heart rate history and are also characterized by rate-independent variability, leading to difficulty in precise rate-correction of the raw QT interval. The present study elucidates a novel analytical method that effectively addresses this problematic phenomenon in telemetered common marmosets. Methods: ECGs were collected from telemetered common marmosets (male and female) and analyzed by computerized algorithms. Descriptive statistics were calculated from the mean of QT intervals for 5-ms increments of RR. The QT interval was corrected for the RR interval by applying Bazett's, Fridericia's, and individual probabilistic QT rate-correction formulae. Results: The linear regression of log-transformed QT and RR intervals derived from a probabilistic approach yielded a well-correlated QT–RR fit. Assessed as the slope of the QTc–RR interval, application of individual probabilistic QT rate-corrections resulted in the most effective dissociation of the effects of rate from the raw QT interval, compared to generic rate-correction formulae. Using individual corrections, the QTc was stable while the interquartile range (IQR) of the QTc distribution was stable, spanning 5–10 ms for each subject over all physiological RR intervals. Heart rate variability distributions were centered about unity during both photoperiods and sinus arrhythmia was far less pronounced compared with measurements in dogs. Discussion: Probabilistic QT rate-correction eliminated the confounding effects of heart rate and provided a stable QTc baseline. These results indicate that application of this method of analysis in telemetered common marmosets results in a high degree of sensitivity for the consistent detection of small (5–10 ms) changes in the QTc interval.
The QT interval: Too long, too short or just right
2009, Heart Rhythm
Citation Excerpt :
Consequently, there is little change in the uncorrected QT interval as the R-R interval shortens and lengthens with respiration, often leading to “long” QTc during sinus rate acceleration and normal QTc during deceleration. One study (not confirmed with genetic data) suggests that QTc ≥460 ms during the shortest R-R interval, or marked variability (>40 ms) of the uncorrected QT during sinus arrhythmia, favors the diagnosis of LQTS.15 QTc values ≥450 ms for males and ≥460 ms for females are noteworthy because 90% of LQTS patients, but only 10% of healthy individuals, have longer QT intervals (remember the caveat of sinus tachycardia).
Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome
2001, Cell
Andersen's syndrome is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. We have mapped an Andersen's locus to chromosome 17q23 $maximum LOD = 3.23 at θ = 0$ near the inward rectifying potassium channel gene KCNJ2. A missense mutation in KCNJ2 (encoding D71V) was identified in the linked family. Eight additional mutations were identified in unrelated patients. Expression of two of these mutations in Xenopus oocytes revealed loss of function and a dominant negative effect in Kir2.1 current as assayed by voltage-clamp. We conclude that mutations in Kir2.1 cause Andersen's syndrome. These findings suggest that Kir2.1 plays an important role in developmental signaling in addition to its previously recognized function in controlling cell excitability in skeletal muscle and heart.
Normal and abnormal QT interval duration and its changes in preadolescents and adolescents practicing sport
2019, Europace

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¹: Dr. Martin's current address is: University of Nebraska Medical Center, 600 South 42nd Street, Omaha, Nebraska 68198.

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Brief reportCalculation of QTc duration and variability in the presence of sinus arrhythmia

Am Heart J

J Am Coll Cardiol

Delayed repolarization (QT or QTu prolongation) and malignant ventricular arrhythmias

Mod Concepts Cardiovasc Dis

The long QT syndrome

Brief report
Calculation of QTc duration and variability in the presence of sinus arrhythmia